ArticleAlcoholism, clinical and experimental research2017
Sedative and Motor Incoordination Effects of Ethanol in Mice Lacking CD14, TLR2, TLR4, or MyD88.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
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- Toll-Like Receptor 4 Signaling and Drug Addiction.Frontiers in pharmacology · 2020Review
- Role of MyD88 in IL-1β and Ethanol Modulation of GABAergic Transmission in the Central Amygdala.Brain sciences · 2019Article
- Toll-like receptor 3 dynamics in female C57BL/6J mice: Regulation of alcohol intake.Brain, behavior, and immunity · 2019Article
- Toll-like receptor 3 activation increases voluntary alcohol intake in C57BL/6J male mice.Brain, behavior, and immunity · 2019Article
- Interactions between TLR4 methylation and alcohol consumption on subjective responses to an alcohol infusion.Alcohol and alcoholism (Oxford, Oxfordshire) · 2018Article
- Role of TLR4 in the Modulation of Central Amygdala GABA Transmission by CRF Following Restraint Stress.Alcohol and alcoholism (Oxford, Oxfordshire) · 2018Article
- Apremilast Alters Behavioral Responses to Ethanol in Mice: II. Increased Sedation, Intoxication, and Reduced Acute Functional Tolerance.Alcoholism, clinical and experimental research · 2018Article
- Ethanol Consumption in Mice Lacking CD14, TLR2, TLR4, or MyD88.Alcoholism, clinical and experimental research · 2017Article
- Genetic and Pharmacologic Manipulation of TLR4 Has Minimal Impact on Ethanol Consumption in Rodents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn our companion article, we examined the role of MyD88-dependent signaling in ethanol (EtOH) consumption in mice lacking key components of this inflammatory pathway and observed differential effects on drinking. Here, we studied the role of these same signaling components in the acute sedative, intoxicating, and physiological effects of EtOH. Toll-like receptor 4 (TLR4) has been reported to strongly reduce the duration of EtOH-induced sedation, although most studies do not support its direct involvement in EtOH consumption. We examined TLR4 and other MyD88 pathway molecules to determine signaling specificity in acute EtOH-related behaviors. We also studied other GABAergic sedatives to gauge the EtOH specificity and potential role for GABA in EtOH's sedative and intoxicating effects in the mutant mice.
methodsLoss of righting reflex (LORR) and recovery from motor incoordination were studied following acute injection of EtOH or other sedative drugs in male and female control C57BL/6J mice versus mice lacking CD14, TLR2, TLR4 (C57BL/10ScN), or MyD88. We also examined EtOH-induced hypothermia and blood EtOH clearance in these mice.
resultsMale and female mice lacking TLR4 or MyD88 showed reduced duration of EtOH-induced LORR and faster recovery from EtOH-induced motor incoordination in the rotarod test. MyD88 knockout mice had slightly faster recovery from EtOH-induced hypothermia compared to control mice. None of the mutants differed from control mice in the rate of blood EtOH clearance. All of the mutants showed similar decreases in the duration of gaboxadol-induced LORR, but only mice lacking TLR4 were less sensitive to the sedative effects of pentobarbital. Faster recovery from diazepam-induced motor impairment was observed in CD14, TLR4, and MyD88 null mice of both sexes.
conclusionsTLR4 and MyD88 were key mediators of the sedative and intoxicating effects of EtOH and GABAergic sedatives, indicating a strong influence of TLR4-MyD88 signaling on GABAergic function. Despite the involvement of TLR4 in EtOH's acute behaviors, it did not regulate EtOH consumption in any drinking model as shown in our companion article. Collectively, our studies demonstrate differential effects of TLR-MyD88 components in the acute versus chronic actions of EtOH.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.